Chronic and acute inflammatory conditions form the basis for diseases affecting all organ systems including, but not limited to, asthma, acute inflammatory diseases, vascular inflammatory disease, chronic inflammation, atherosclerosis, angiopathy, myocarditis, nephritis, Chron's disease, arthritis, type I and II diabetes and associated vascular pathologies. The incidence of these inflammatory conditions is on the rise in the population as a whole, with diabetes alone affecting 16 million people.
While inflammation in and of itself is a normal immune response, chronic inflammation leads to complications and ongoing system damage due to the interactions of unknown cellular factors. In particular, chronic inflammation can cause endothelial damage resulting in vascular complications. Coronary artery, cerbrovascular and peripheral vascular disease resulting from atherosclerotic and thromboembolic macroangiopathy are the primary causes of mortality in chronic inflammatory diseases. (1, 2)
Inflammation is maintained by inflammatory cytokines which increase production of growth promoting genes by vascular cells and leukocytes leading to increased lesion formation in blood vessels. IL-1, for example, increases the production of platelet derived growth factor A chain (PDGF) by smooth muscle cells. PDFG induces proliferation of fibroblasts, microglia, and smooth muscle. PDGF may also serve as a chemotactic agent for inflammatory cells, thereby continuing the cycle and leading to further damage.
Though currently there are pharmaceutical agents directed to treating inflammatory conditions, none of these agents are capable of specifically controlling cellular components triggered by inflammatory responses or components that are the triggering agent for inflammation. What is needed are compositions and methods that specifically target cellular components of inflammation to treat diseases and conditions that are caused by or lead to inflammatory states.